Most infrarenal AAAs (66%) can be treated with endovascular devices currently available commercially or through US Food and Drug Administration-approved clinical trials. However, patients who are at high risk for surgery and might benefit most from endovascular repair are less likely to qualify for the procedure (49%). Men (70%) are more likely than women (40%) to meet the anatomic criteria for endografting. Difficulties with vascular access and attachment site geometry predominate as reasons for exclusion. Our findings suggest that smaller profile devices, which can negotiate small and tortuous iliac arteries, are needed. Proximal and distal attachment site problems require devices that can accommodate wide and angulated attachment necks and achieve short seal zones.

ClinicalTrials.gov; No.: NCT01854645 and No. NCT01854658; URL: www.clinicaltrials.gov.

It is possible to measure pressures from within the aneurysm sac in patients with stent grafts with a variety of techniques. Patients may continue to have pressurized AAA sacs despite endovascular AAA repair. Endoleaks transmit pulsatile pressure into the aneurysm sac regardless of the type. It is possible to have systemic sac pressures without evidence of endoleaks on CT or angiography.

Emerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistochemical data were analyzed using a chi(2)-test. PF4 was detected in the cytoplasm of luminal and neovascular endothelium, in macrophages and in regions of plaque calcification. The presence of PF4 in macrophages and neovascular endothelium correlated with lesion grade (p = 0.004; p = 0.044). Staining of macrophages for PF4 correlated with the presence of symptomatic atherosclerotic disease (p = 0.028). In early lesions, PF4 was commonly found in macrophages of early lesions (Grade I/II), whereas NAP-2 was rarely present. In conclusion, correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis suggests that persistent platelet activation may contribute to the evolution of atherosclerotic vascular lesions. These studies support the rationale for the chronic use of anti-platelet therapy in patients at risk for developing symptomatic atherosclerosis.

The transarterial embolization of inferior mesenteric arteries for the repair of type 2 endoleaks is ineffective and should not be performed. Direct translumbar embolization of the endoleak is effective in the elimination of type 2 leaks and should be the therapy of choice when aggressive endoleak management is indicated.